Biomedical subjects

Tao Lin

Publications and source records attributed to Tao Lin.

At least 19 recordsLinked to original sources

PubMed2024

The genomic route to tomato breeding: Past, present, and future.

Over the past 10,000 years, tomato species have undergone both unintentional and intentional selection to enhance their favorable traits for human consumption and manufacturing. These selection processes have significantly influenced the genomes of tomato species and have played a critical role in improving tomato varieties. In this review, we summarize recent advances in tomato genome sequencing, explore the impact of human-driven selection, and recapitulate key genes associated with important agronomic traits in tomato breeding. We provide several examples of genomics-guided tomato breeding to highlight the potential of genome resources in facilitating tomato improvement. Furthermore, we elaborate the progress and strategies of tomato breeding through genome design and present how such efforts can help future enhancements of tomato to align with the demands of sustainability and evolving human societies.

Solanum lycopersicum↗

PubMed2024

Clinical efficacy of thalidomide for various genotypes of beta thalassemia.

OBJECTIVE: The objective of this study was to investigate the therapeutic efficacy of thalidomide across various genotype presentations of β-thalassemia so as to facilitate the early screening of thalidomide-sensitive thalassemia cases and to understand the impact of iron overload on thalidomide. METHODS: From our initial sample of 52 patients, we observed 48 patients with β-thalassemia for two years after administration of thalidomide. This cohort included 34 patients with transfusion-dependent thalassemia (TDT) and 14 patients with non-transfusion-dependent thalassemia (NTDT). We recorded the values of hemoglobin (Hb), fetal hemoglobin (HbF), and serum ferritin (SF) in the baseline period and at 1, 3, 6, 12, 18, and 24 months after enrollment, as well as the pre- and post-treatment blood transfusion volume in all 48 cases. According to the increase in Hb levels from baseline during the 6-month observation period, the response to thalidomide was divided into four levels: main response (MaR), minor response (MiR), slow response (SLR), and no response (NR). A decrease in serum ferritin levels compared to baseline was considered alleviation of iron overload. We calculated the overall response rate (ORR) as follows: ORR = MaR + MiR + SLR/number of observed cases. RESULTS: The ORR was 91.7% (44/48 cases), and 72.9% showed MaR (35/48 cases). Among the 34 patients with TDT, 21 patients (61.8%) were free of blood transfusion, and the remaining 13 patients still required blood transfusion, but their total blood transfusion volume reduced by 31.3% when compared to the baseline. We found a total of 33 cases with 10 combinations of advantageous genes, which included 5 cases with βCD41-42/βCD17 and 6 cases with βCD41-42/β-28. Based on the treatment outcomes among the 48 cases in the observation group, there were 33 cases in the MaR group and 15 cases in the SLR/NR group. There was a difference in HbF between the two groups at baseline (P = 0.041). There were significant differences between the two groups in Hb and HbF at the time points of 6 and 12 months, respectively (P < 0.001). Compared to the baseline measurement, there was a significant decrease in the level of SF at months 12 and 24 (P < 0.001). CONCLUSION: In this study, we identified 10 β-thalassemia gene combinations that were sensitive to thalidomide. These gene combinations can be used for initial screening and to predict the therapeutic effect of thalidomide in clinical practice. We examined the therapeutic response to thalidomide and found that the administration of thalidomide in combination with standardized iron removal was more beneficial in reducing iron overload.

Humans↗

PubMed2006

Cytoskeleton vimentin disruption of mouse sertoli cells injured by nitrogen mustard in vitro.

Reproductive toxicity is one of the potential side effects of anticancer alkylating agents, with potential effects on vimentin intermediate filaments, one of the main components of the Sertoli cytoskeleton. Research suggests (Aumuller et al, 1988; Aumuller et al, 1992) that the highly organized and active Sertoli cytoskeleton is important in spermatogenesis. The aim of the current study was to investigate the effects of alkylating agents on vimentin filament expression in vitro. Sertoli cells, isolated from 20-day-old mice testes, were cultured for 5 days and then incubated with 0, 50, 100, and 200 micromol/L nitrogen mustard (HN2). Morphologic changes in Sertoli cells were observed per 30-minute interval at 12-hour exposure time points to 100 micromol/L HN2. Vimentin expression was investigated by immunocytochemistry at 6 hours and 24 hours posttreatment and reverse transcriptase polymerase chain reaction and Western blot at 12 hours posttreatment with 50, 100, and 200 micromol/L HN2. Exposure to HN2 resulted in a comparatively small Sertoli cell body with diminished cytoplasm. Sertoli cells were shrunk or detached. Cytoskeletal disruption increased with increasing HN2 concentration. The optical density values of vimentin antibody and expression of vimentin mRNA and protein were significantly decreased with increasing concentration of HN2. Significant treatment dose-dependent and time-dependent differences of vimentin mRNA and protein expression levels were also noted. Our data suggest that the change in the biochemical properties of vimentin may indicate that one of the mechanisms of reproductive toxicity resulting from HN2 is disruption of Sertoli cell vimentin filament structure, accompanied by a down-regulation of vimentin expression.

Alkylating Agents↗

PubMed2006

Efficient hepatocyte engraftment in a nonhuman primate model after partial portal vein embolization.

BACKGROUND: Hepatocyte transplantation could be an alternative to whole liver transplantation for the treatment of metabolic liver diseases. However, the results of clinical investigations suggest that the number of engrafted hepatocytes was insufficient to correct metabolic disorders. This may partly result from a lack of proliferation of transplanted hepatocytes. In rodents, portal ligation enhances hepatocyte engraftment after transplantation. We investigated the effects of partial portal ligation and embolization on engraftment and proliferation of transplanted hepatocytes in primates. METHODS: Hepatocyte autotransplantation was performed in Macaca monkeys. The left lateral lobe was resected for hepatocyte isolation. The first group of monkeys underwent surgical ligation of the left and right anterior portal branches; in the second group, the same portal territories were obstructed by embolization with biological glue. To evaluate the proportion of cell engraftment hepatocytes were Hoechst-labeled and transplanted via the portal vein. Cell proliferation was measured by BrdU incorporation. RESULTS: Hepatocyte proliferation was induced by both procedures but it was significantly higher after partial portal embolization (23.5% and 11.2% of dividing hepatocytes on days 3 and 7) than after ligation (3% and 0.8%). Hepatocytes engrafted more efficiently after embolization than after ligation. They proliferated and participated to liver regeneration representing 10% of the liver mass on day seven and their number remained constant on day 15. CONCLUSIONS: These data suggest that partial portal embolization of the recipient liver improves engraftment of transplanted hepatocytes in a primate preclinical model providing a new strategy for hepatocyte transplantation.

Animals↗

PubMed2006

[Application of magnetoencephalography localization in brain tumor surgery].

OBJECTIVE: To evaluate the applied value of magnetoencephalography (MEG) localization in microsurgery of brain tumors in the region of motor cortex. METHODS: From January 2003 to April 2005, 36 patients with 19 meningomas, 14 gliomas, 2 metastases and 1 cavernous angioma underwent MEG and MRI before operation. These individualized functional brain maps were integrated into a neuronavigation system. Preoperative mapping of somatosensory and/or motor cortex was performed, and sites were compared, and all tumors were resected microsurgerically. RESULTS: A space-occupying lesion could change the region of motor cortex in all the patients. Thirty-four cases were resected totally. The patient's myodynamia after operation improved in 19 cases, unchanged in 15 cases, descended in 2 cases. CONCLUSIONS: MEG is an effective localization method of function, providing the relationship between the region of motor cortex and the tumor. And it is valuable for accurate planning in the treatment of brain tumors in the region of motor cortex.

Adolescent↗

PubMed2006

Screening and identification of vascular-endothelial-cell-specific binding peptide in gastric cancer.

Antiangiogenesis therapy has become a hot field in cancer research. Blood vessels of tumor carry specific markers that are usually related to angiogenesis. Study of these heterogeneous molecules in different tumor vessels may be beneficial for promoting antiangiogenic therapy. In this study, we established an in vitro co-culture model of human umbilical vein endothelial cells (HUVECs) and gastric adenocarcinoma cell line SGC7901, screened the peptides binding specifically to the HUVECs co-cultured with gastric cancer cells (Co-HUVECs) using phage display peptides library, and studied the affinity of these peptides to gastric cancer vascular endothelial cells. After four rounds of panning, there was an obvious enrichment for the phages specifically binding to the Co-HUVECs, and the output/input ratio of Co-HUVECs increased about 590-fold (from 0.95x10(-7) to 561.25x10(-7)). Five phage clones (M6, M3, M9, IN12, IN11), which could strongly bind to Co-HUVECs instead of wild-type HUVECs, were characterized by ELISA. In vitro cellular binding assay showed that phage IN11 preferably bound to Co-HUVECs rather than control HUVECs, and the number of the phage IN11 recovered from Co-HUVECs was 5.7- and 16.9-folds, respectively, as much as those from control HUVECs and GES cells. Immunocytochemical and immunohistochemical staining confirmed that phage IN11 could specifically bind to Co-HUVECs as well as vascular endothelial cells in gastric cancer tissue sections. Competitive and inhibitory assay revealed the synthetic peptide GEBP11 (CTKNSYLMC) displayed on phage IN11 could competitively inhibit binding of the phage IN11 to Co-HUVECs. Immunofluorescence microscopy showed that the fluorescence-labeled peptide GEBP11 was located at the membrane and perinuclear cytoplasm of Co-HUVECs. Meanwhile, GEBP11 was found to be able to target the gastric cancer vascular endothelial cells. Therefore, GEBP11 may be a potential candidate for targeted drug delivery in antivascular therapy and diagnosis of gastric cancer.

Amino Acid Sequence↗

PubMed2006

Local extravascular pool of C3 is a determinant of postischemic acute renal failure.

The third complement component (C3) is an acute phase protein that plays a central role in reperfusion injury in several organ models. To investigate the contribution of local synthesis of C3 and distinguish it from that of circulating complement mainly produced by hepatic synthesis, we employed a mouse renal isograft model. Our model demonstrated a close relationship between the extent of intrarenal expression of C3 and cold-ischemia induced injury. Ischemic C3-positive donor kidneys transplanted into C3-positive or C3-negative recipients developed widespread tissue damage and severe acute renal failure. In contrast, ischemic C3-negative isografts exhibited only mild degrees of functional and structural disturbance, even when transplanted into normal C3-positive recipients. Thus local synthesis of C3, mostly identified in the tubular epithelium, was essential for complement-mediated reperfusion damage, whereas circulating C3 had a negligible effect. Our results suggest a two-compartment model for the pathogenic function of C3, in which the extravascular compartment is the domain of local synthesis of C3, and where the role of circulating C3 is redundant. Our data cast new light on the mechanism of complement-mediated tissue injury in nonimmunological disorders, and challenges the longstanding dogma that circulating components are the main complement effectors of extravascular tissue damage.

Animals↗

PubMed2006

ZNRD1 mediates resistance of gastric cancer cells to methotrexate by regulation of IMPDH2 and Bcl-2.

We previously showed that downregulation of a transcription-associated gene (ZNRD1) could reverse the resistant phenotype of gastric cancer cells through regulation of the transcription of multidrug resistance gene 1 (MDR1). In the present study, we determined both known and novel differentially expressed genes in VCR-induced multidrug resistant gastric cancer cell SGC7901/VCR transfected with ZNRD1 siRNA or empty vector control. Screening was performed using the Human Cancer Xpro(tm) HC-III plus arrays, containing 3072 cancer-related cDNAs. Ten genes, involved in cell cycle control, nucleic acid binding, and protein phosphorylation, among other functions, underwent more than 5-fold change. Of the downregulated genes we chose Inosine monophosphate dehydrogenase 2 (IMPDH2) for further validation by quantitative RT-PCR. In vitro and in vivo drug sensitivity analyses revealed that inhibition of ZNRD1 and IMPDH2 activity sensitized SGC7901/VCR cells to methotrexate. Additionally, inhibition of ZNRD1 could suppress adriamycin-induced apoptosis and significantly downregulate the expression of Bcl-2, but it did not alter the expression of the glutathione-S-transferase, or intracellular glutathione content. Taken together, the findings suggest that ZNRD1 could act as a modulator of methotrexate chemotherapy in gastric cancer cells through the regulation of IMPDH2 and Bcl-2.

Antimetabolites, Antineoplastic↗

PubMed2006

Study of removal effect on Mesocyclops leukarti with oxidants.

Cyclops of zooplankton propagates prolifically in eutrophic waterbody and it cannot be exterminated by conventional disinfection process. The mutagenicity of Mesocyclops leukarti and its extermination with oxidants in a drinking waterworks in China were studied. Among five oxidants for use in bench-scale, chlorine dioxide is the most effective and the potassium permanganate is the weakest against Mesocyclops leukarti under the same conditions. Full-scale results showed that Mesocyclops leukarti could be effectively removed from water by 1.0 mg/L chlorine dioxide preoxidation combined with conventional removal physical process. After filtration, chlorite, a by-product of prechlorine dioxide, is stable at 0.45 mg/L, which is lower than the critical value of the USEPA. GC-MS examination and Ames test further showed that the quantity of organic substance and the mutagenicity in water treated by chlorine dioxide preoxidation are obviously less than those of prechlorination.

Copepoda↗

PubMed2006

Deficiency of C4 from donor or recipient mouse fails to prevent renal allograft rejection.

Complement effector products generated in the transplanted kidney are known to mediate transplant rejection, but which of the three main activation pathways of complement trigger this response is unclear. Here we assessed the role of the classical and lectin pathways by studying the common component C4 in mouse kidney transplant rejection. We transplanted wild-type or C4-null H-2(b) donor kidneys into H-2(k) or H-2(d) recipients, or vice-versa, to assess the roles of donor kidney and recipient expression of complement. Intragraft C4 gene expression rose substantially during rejection. However, we found no significant association between graft acceptance and the presence of C4 in either the donor kidney or recipient mouse. At the time of rejection, we found no significant differences in alloantibody response in the different groups. Tubular deposition of C3 to C9 occurred regardless of the absence or presence of C4 in either the donor or recipient mouse, indicating that C4 was dispensable for complement activation at this site. These data suggest that complement activation and renal allograft rejection are independent of the classical and lectin pathways in these models, implying that in the absence of these pathways the alternative pathway is the main trigger for complement-mediated rejection.

Animals↗

PubMed2006

[Effect of cyclophosphamide on spermatogonial stem cells].

OBJECTIVE: To perform a preliminary study on the dysfunction of spermatogonial stem cells (SSCs) induced by cyclophosphamide. METHODS: According to development stage of spermatogenesis in Wistar rat, 72 rats were divided into three groups, 1, 3 and 9 weeks groups, respectively. Then 24 rats per group were randomly divided into experimental and control groups, and 100 mg/kg cyclophosphamide was injected by intraperitoneal injection in experimental groups, with the same volume of normal saline in the control. Apoptosis of spermatogenic cells were detected after 24 hours by TUNEL. Then 60 one-week rats, whose germ cells were only SSCs, were randomly divided into experimental and control group. We detected c-Kit by immunohistochemistry and cell cycle by flow cytometry at 24 hours, 3 and 9 weeks. RESULTS: There was no significant difference in apoptosis of germ cells in 1 week between experimental group and control group ( P > 0.05); however, there were significant differences among other groups. The ratio of S stage and c-Kit expression of spermatogonial cells were decreased in one-week rats at 24 hours, 3 and 9 weeks in experimental group compared with the control, respectively (P < 0.01). CONCLUSION: Cyclophosphamide does not significantly induce SSCs apoptosis. It may be more important to interfere the proliferation and differentiation of SSCs.

Animals↗

PubMed2005

Celecoxib could reverse the hypoxia-induced Angiopoietin-2 upregulation in gastric cancer.

We investigated the potential effect of Cyclooxygenase-2 (Cox-2) on hypoxia-induced Angiopoietin-2 (Ang-2) expression in gastric cancer cells. Our results revealed that hypoxia augmented Cox-2 and Ang-2 expressions. Also, the hypoxia-induced Ang-2 could be mimicked by CoCl(2) treatment while genestein treatment could partially counteract the hypoxia-induced Ang-2 expression. Celecoxib but not Cox-1 inhibitor sc-560 reversed the hypoxia-induced Ang-2 expression, while this effect could be partially restored by addition of exogenous PGE2. Our findings suggest that the hypoxia-elevated Ang-2 expression in gastric cancer cells may be mediated by both Cox-2-derived PGE2 and HIF-1alpha pathways, while celecoxib could counteract the hypoxia-induced Ang-2 expression.

Angiopoietin-2↗

PubMed2005

Regulation of multidrug resistance by MGr1-antigen in gastric cancer cells.

Previously, a novel protein, MGr1-Ag, was associated with tumor multidrug resistance (MDR), and the role and the underlying mechanisms of MGr1-Ag in MDR of gastric cancer cells were characterized. Initial studies using the introduction of sense or antisense vectors for MGr1-Ag resulted in the genetical up- or downregulation of MGr1-Ag in gastric cancer cells, respectively. Subsequent studies revealed the expression of MGr1-Ag, P-glycoprotein (P-gp), MDR-associated protein (MRP), Bcl-2 and Bax in gastric cancer cells via Western blot analysis. The sensitivity of gastric cancer cells to chemotherapeutic drugs was assessed using the colony-forming assay, and Adriamycin (ADM) accumulation was evaluated by flow cytometry. Further study of ADM-induced apoptosis was detected by annexin-V/propidium iodide staining. The expression level of MGr1-Ag in MDR gastric cancer cells is much higher than that in their parental cells. Overexpression of exogenous MGr1-Ag may promote the MDR phenotype of gastric cancer cells, decrease intracellular ADM accumulation and protect gastric cancer cells from ADM-induced apoptosis, whereas downregulation of MGr1-Ag had reverse effects. Western blot analysis suggested that MGr1-Ag may regulate the expression of P-gp, MRP, Bcl-2 and Bax. In conclusion, MGr1-Ag may promote MDR of gastric cancer cells via a decrease in intracellular drug accumulation and inhibition of drug-induced apoptosis.

Antibiotics, Antineoplastic↗

PubMed2005

[Cognitive function and psychological characteristics of patients with chronic fatigue syndrome].

OBJECTIVE: To investigate the cognitive function and psychological characteristics of the patients with chronic fatigue syndrome (CFS) in China and analyze its relation with primary psychological diseases. METHODS: Ninety-one patients with CFS who visited the People's Hospital, Peking University, in Beijing from Beijing, Shanghai, Tianjin, Heilongjiang, Jilin, Hebei, Inner Mongolia, Shanxi, Shandong, Sichuan, Gansu, Fujian, and Guangdong, 42 males and 49 females, aged 37 +/- 7, 43% of which had the record of formal schooling of regular college course or over and 21 of which had the record of formal schooling of college for professional training, and 58% of which showed clear causes, diagnosed by the CDC criteria 1994, underwent case history collection, physical examination, necessary laboratory test, memory test, and SCL-90, Hamilton depression rating scale (HAMD), and Hamilton anxiety rating scale (HAMA) testing. Thirty healthy persons, 14 males and 16 females, aged 37 +/- 7, were used as controls., A table of case file was established based on the CDC criteria 1994 for each patient to record the relevant data. Independent-Samples T Test was used to compare the memory quotient, the total score and general mean score of SCL-90, the score of HAMD and HAMA. Analyzed the impairment of cognitive function and psychological characteristics of patients with CFS. RESULTS: The most common symptoms was descent of remembrance and/or attention (82/91, 90%). The memory quotient of the CFS patients was 85 +/- 14, significantly lower than that of the healthy controls (98 +/- 12, t = 4.627, P = 0.000). The total score of SCL-90 of the CFS patients was 192 +/- 47, significantly higher than that of the healthy controls (140 +/- 46, t = 5.297, P = 0.000). The symptoms with a factor score > or = 2.0 in SCL-90 included obsessive-compulsive symptoms (61/91, 67%), somatization (61/91, 67 %), depression (57/91, 63%), and anxiety (49/91, 54%). The HAMD score of the CFS patients was 9.9 +/- 6.1, significantly higher than that of the healthy controls (6.5 +/- 2.5, t = 2.948, P = 0.004). The HAMA score of the CFS patients was 9.9 +/- 7.0, significantly higher than that of the healthy controls (5.9 +/- 2.9, t = 3.015, P = 0.003). CONCLUSION: The CFS patients in China have an obvious impairment of remembrance and show different psychological abnormalities that are different from those of the patients with primary psychological diseases.

Adult↗

PubMed2005

Determination of promethazine hydrochloride and its preparations by highly accurate nephelometric titration.

A highly accurate nephelometric titration for the determination of promethazine hydrochloride and its preparations was presented. The titration operating conditions were studied and the solubility product constant of promethazine tetraphenylboron precipitation was determined. The result of the titration is comparable to those of control experiments. The proposed method has been found to be accurate, precise, specific and linear.

Nephelometry and Turbidimetry↗

PubMed2005

Identification and characterization of a novel water-deficit-suppressed gene OsARD encoding an aci-reductone-dioxygenase-like protein in rice.

The aci-reductone dioxygenase (ARD) family common to bacteria, plants and animals is involved in the methionine salvage pathway. A water-deficit-suppressed gene, OsARD encoding an aci-reductone-dioxygenase-like protein, was identified from rice (Oryza sativa L.). Northern blot and reverse transcriptase-polymerase chain reaction (RT-PCR) analysis revealed that the OsARD expression is regulated by abiotic stresses and phytohormones. OsARD was mainly expressed in roots under flood conditions. It was suppressed by abiotic stresses including water deficit, high salinity and low temperature, and induced by ethylene and gibberellin acid (GA). Our results showed that the genes for S-adenosylmethionine (SAM) synthase and 1-aminocyclopropane-1-carboxylic acid (ACC) synthase were upregulated in RNA-interference (RNAi) transgenic rice plants with a significant reduction of OsARD expression. Furthermore, the expression of two genes for ethylene signal transduction, ETR2 and EIN3, increased in these RNAi transgenic plants, whereas the expression of ERF3 was suppressed. These results suggest that OsARD may play a role in the metabolism of methionine and ethylene in response to abiotic stresses.

Amino Acid Sequence↗

PubMed2005

Tumor suppressor gene Runx3 sensitizes gastric cancer cells to chemotherapeutic drugs by downregulating Bcl-2, MDR-1 and MRP-1.

The Runx3 gene is a member of the runt domain family transcription factors, key regulators of development and differentiation in metazoan. Recently, Runx3 was identified as a tumor suppressor gene. Loss of Runx3 was found to be associated with genesis and progression of gastric cancer. In this study, we transfected the gastric cancer cell line SGC7901 with eukaryotic expression vector of Runx3. In vitro drug sensitivity assay suggested that SGC7901/Runx3 cells were more sensitive to various chemotherapeutic drugs. Blocking Runx3 expression in immortalized stomach mucosal cells (GES-1) or gastric cancer cells (SGC7901) by Runx3-specific small interfering RNA conferred the cells resistance to chemotherapeutic drugs. Flow cytometry examination suggested that expression of Runx3 in gastric cancer cells increased the intracellular accumulation and retention of adriamycin. Semiquantitative RT-PCR and Western blot suggested that Runx3 downregulated expression of Bcl-2, MDR-1 (P-gp) and MRP-1. Binding of Runx3 to promoter sequences of Bcl-2, MDR-1 and MRP-1 gene was detected by eletrophoretic mobility shift assay (EMSA) and supershift EMSA. We cloned the MDR-1 and MRP-1 gene promoters containing Runx binding sites and constructed the luciferase reporter vectors of these 2 promoters. Luciferase reporter assay suggested that Runx3 inhibited the promoter activity of the MDR-1 and MRP-1 promoter in SGC7901 cells. Taken together, our findings suggested that overexpression of Runx3 could sensitize gastric cancer cells to chemotherapeutic drugs by downregulating the Bcl-2, MDR-1 and MRP-1.

Adenocarcinoma↗

PubMed2005

A novel DNA vaccine containing four mimicry epitopes for gastric cancer.

Gastric cancer is one of the most common malignant tumors in China. This paper focuses on the development of a DNA vaccine containing four mimotopes of MG7Ag for gastric cancer (multi-epitope vaccine). By inoculating BALB/c mice, the vaccine was characterized and compared with a similar vaccine containing only one mimotope (mono-epitope vaccine) and other controls. Cellular ELISA indicated that serum titer of antibody against MG7Ag was significantly higher in mice immunized with the multi-epitope vaccine than that in the group immunized with the mono-epitope vaccine (0.8627 vs 0.6754, P < 0.05). And ELISPOT assay showed that the number of INF-gamma spots induced by multi-epitope vaccine was significantly larger than that of the group immunized with mono-epitope vaccine(93.3 vs 70.7, P < 0.05). Two weeks after tumor challenge, the weight of tumor in each mouse was evaluated, and the tumor masses formed in the mice immunized with multi-epitope vaccine were markedly smaller than those formed in the mice immunized with mono-epitope vaccine. These studies demonstrated that both humoral and cellular response were induced by the two vaccines and the efficiency of multi-epitope vaccine is stronger than that of the mono-epitope vaccine.

Amino Acid Sequence↗